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Pharmacology II > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

What is the lack of oxygen and reduced blood flow to the myocardium resulting in an imbalance between myocardial oxygen supply and demand?

A

Ischemia

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2
Q

What is necrosis (death) of heart muscle caused by an imbalance between oxygen supply and demand?

A

Infarction

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3
Q

What is “chest pain”; pain or discomfort in the chest or adjacent areas which is due to myocardial ischemia?

A

Angina Pectoris

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4
Q

What is a painless episodes of myocardial ischemia (75% of all ischemia)?

A

Silent ischemia

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5
Q

What is an infarction occurring without chest pain or other common symptoms of ischemia; about 20% of all infarcts?

A

Silent infarction

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6
Q

What is unstable angina or acute myocardial infarction?

A

Acute coronary syndrome

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7
Q

Acute coronary syndromes include?

A 
Unstable angina (UA)
Myocardial infacrtion (MI)
Cardiovascular disease (CVD)
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8
Q

What is the leading cause of death in the US?

A

Cardiovascular dz

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9
Q

Acute coronary syndrome is a form of what? Which comprises the most common cause of CVD death?

A

Coronary heart disease (CHD)

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10
Q

What are the risk factors of CHD?

A
  • Family history
  • Obesity
  • Elevated C-reactive protein
  • Sedentary lifestyle
  • Male gender
  • Stressful lifestyle
  • Hypertension
  • Age
  • Diabetes mellitus
  • Smoking
  • Dyslipidemia
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11
Q

What are the ECG findings for a STEMI?

A
  • Typically results in an injury that transects the thickness of the myocardial wall
  • Following an MI pathologic Q-waves are seen on ECG
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12
Q

What are the ECG findings for NSTEMI?

A
  • Limited to sub-endocardial myocardium
  • Patients do not usually develop pathologic Q-wave
  • Differs from unstable angina in that ischemia is severe enough to produce myocardial necrosis
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13
Q

What are the causes of Acute Coronary Syndrome?

A
  • -Rupture of an atherosclerotic plaque with subsequent: (blocks of the blood flow and tissue dies): Platelet adherence, activation, and aggregation, Activation of the clotting cascade.
  • -Ultimately a clot forms composed of fibrin and platelets
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14
Q

What is ventricular remodeling?

A
  • -Following an MI ventricular remodeling can occur.
  • -Characterized by left ventricular dilation and reduced pumping function of left ventricle leading to cardiac failure.
  • -Preventing this is an important therapeutic goal following an MI as heart failure represents a principle cause of mortality and morbidity post MI.
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15
Q

Do we want ventricular remodeling to occur?

A

No

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16
Q

What are the symptoms for acute coronary syndrome?

A

–Midline anterior anginal chest discomfort
Most often when at rest
Severe new onset or increasing angina lasting at least 20 min
Chest discomfort may radiate down left arm or to the back or jaw
–N/V
–Diaphoresis
–SOB

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17
Q

When should a 12-lead ECG be obtained?

A

12-lead ECG should be obtained within 10 min of presentation with symptoms of ischemic chest discomfort (this is the goal)

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18
Q

What are the key findings of myocardial ischemia or infarction?

A

STE
ST-segment depression
T-wave inversion
Appearance of a new left bundle-branch block + chest pain highly specific for acute MI

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19
Q

What are biochemical markers important for?

A

Confirming diagnosis of MI

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20
Q

What biochemical markers rise following myocardial cell death?

A

Troponin and CK-MB

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21
Q

When are blood samples obtained for suspected MI?

A

3 times over 12-24 hours.

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22
Q

What biochemical markers determine an MI?

A

MI identified if at least 1 troponin value or 2 CK-MB values are greater thet the MI decision limit

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23
Q

Does unstable angina have elevated cardiac enzymes? ST-segment elevation?

A

Elevated cardiac enzymes- No

ST-segment elevation- NO

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24
Q

Does non-ST-elevation MI have elevated cardiac enzymes? ST-segment elevation?

A

Elevated cardiac enzymes- Yes

ST-segment elevation- No

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25
Q

Does ST-elevation MI have elevated cardiac enzymes? ST-segment elevation?

A

Elevated cardiac enzymes- Yes

ST-segment elevation- Yes

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26
Q

What patients are at highest risk of death?

A

Those with ST- elevation

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27
Q

What is the risk stratification for NSTEMI?

A

High risk–TIMI score 5-7 points
Medium risk–TIMI score 3-4 points
Low risk –TIMI score 0-2 points

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28
Q

What are the general treatment principles to reduce myocardial oxygen demand?

A
  • Lower heart rate
  • Lower systolic blood pressure
  • Ease cardiac contractility
  • Reduce left ventricle dimension (preload)
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29
Q

What are the general treatment principles to improve myocardial oxygen supply?

A
  • Dilate coronary arteries
  • Enhance coronary blood flow; reduce clot size
  • Reduce left ventricular end-diastolic pressure
  • Prolong diastole (increased coronary perfusion)
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30
Q

What are the general management goals for STEMI and high/intermediate risk NSTE patients?

A
  • Decrease mortality
  • Establish balance between oxygen supply and demand (reverse ischemia) to relieve symptoms
  • Reverse ischemia to prevent necrosis or limit infarct size and decrease complications
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31
Q

What are the general measures for STEMI and high/intermediate risk NSTE patients?

A
  • Oxygen- every patient should be placed on this due to once of our goals being increase ox.
  • Stool softeners- important so that patients arent straining while having an MI this will make it worse
  • Bedrest
  • Diet- no sodium
  • Anxiolytics- really anxious so help with the anxiety
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32
Q

What is PCI?

A

Percutaneous coronary intervention
PCI is a stent that is placed (usually drug eluting, will help to stop the progression of the plaque and buildup and remodeling) this breaks up the clot and allows for good blood flow to the tissue.

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33
Q

What does PCI involve?

A

Percutaneous Transluminal Coronary Angioplasty (PTCA) with coronary stent placement
–1-2 vessel disease or proximal stenosis
Initial success rate 80-90% for opening vessels
–Drug-eluting stents have been shown to reduce restenosis rates
–Contain drugs which inhibit smooth muscle cell proliferation and inflammatory cell activity

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34
Q

When should primary PCI be used?

A

If primary PCI is feasible and can be performed quickly it is generally preferred over fibrinolytic therapy for treating acute STEMI

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35
Q

What is DCA?

A

Direct coronary atherectomy

The excision of atherosclerotic plaque using rotating blades

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36
Q

What does coronary artery bypass grafting (CABG) do?

A

Improves survival in high risk patients

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37
Q

What patients benefit from a CABG?

A
  • -Significant stenosis of left main coronary artery
  • -Proximal LAD stenosis and proximal left circumflex stenosis > 70%
  • -Triple vessel disease
  • -Impaired left ventricular function
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38
Q

What medications are used in MI?

A
  • Nitrates- Nitroglycerin
  • Analgesics
  • Fibrinolytics (Thrombolytics)
  • Antiplatelet drugs
  • Anticoagulants
  • Beta Blockers
  • ACE Inhibitors
  • Calcium Channel Blockers
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39
Q

Nitrates- Pharmacological effects

A
  • direct vasodilators of veins (low dose) and arteries (high dose)
  • venodilation = ↓ preload = ↓ wall tension and -ventricular dimensions
  • dilate epicardial vessels and ↑ blood flow to collateral vessels
  • alleviate coronary spasm
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40
Q

Nitrates- uses

A

Ischemic heart disease
Heart failure
Hypertensive emergencies

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41
Q

Nitrates- Ischemic heart disease MOA

A
  • anti-anginal
  • increases coronary blood flow to the heart
  • reduces cardiac workload
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42
Q

Nitrates- heart failure MOA

A
  • reduces cardiac workload by reducing preload

- typically used in conjunction with an afterload–reducing agent (esp.hydralazine)

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43
Q

Nitrates- Hypertensive emergencies MOA

A
  • vasodilator; quickly reduces blood pressure

- only the intravenous form is used for blood pressure reduction

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44
Q

Nitrates- tolerance mchanisms

A
  • True mechanism unknown; some hypotheses:
  • Sulfhydryl group depletion
  • Activation of the sympathetic nervous system
  • Na and H2O retention = plasma volume expansion
  • Deactivation of nitric oxide by superoxide free radicals
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45
Q

Nitrates- Prevention

A
  • 10-14 hour nitrate-free interval

- Use nitrates cautiously as monotherapy since angina may occur during the nitrate-free period

46
Q

Nitrates- Adverse effects

A
  • Headache (frequently dose-limiting)
  • Syncope and hypotension (potentiated by alcohol, hot weather, or hot bath)
  • Dizziness
  • Tachycardia (rebound)
47
Q

Nitrates- patient counseling

A
  • Keep nitrates stored in airtight containers in a dark, cool, dry place
  • Caution when standing, may precipitate lightheadedness
  • Seek immediate medical attention if pain not relieved within 5 minutes by one SL tablet
  • Dry mouth may slow disintegration of SL tablets
  • Remove patch for 10-12 hours each day to provide a nitrate-free interval and use a new patch each day
  • Replace SL NTG vials every 6 months
48
Q

Nitrates- contraindications

A
  • Severe bradycardia ( < 50 bpm)
  • Tachycardia (> 100 bpm)
  • SBP < 90 mmHg or > 30 mmHg below baseline
  • Should not be administered to patients who have received a phophodiesterase inhibitor!
  • -Within 24h of Sildenafil
  • -Within 48 h of Tadalafil
49
Q

What are the patient characteristics for invasive treatment of NSTEMI and STEMI?

A
  • Recurrent angina or Recurrent angina or ischemia at rest or with low-level activities despite intensive medical therapy
  • Elevated cardiac biomarkers (TnT or TnI)
  • New or presumably new ST-segment depression
  • Signs or symptoms of HF or new or worsening mitral regurgitation
  • High-risk findings from noninvasive testing
  • Hemodynamic instability
  • Sustained ventricular tachycardia
  • PCI within 6 months
  • Prior CABG
  • High risk score
  • Reduced left ventricular function (LVEF less than 40%)
50
Q

What are the patient characteristics for conservative treatment of NSTEMI and STEMI?

A
  • Low risk score

- Patient or physician preference in the absence of high-risk features

51
Q

What is the ACC/AHA classification scheme class I?

A

Benefit&raquo_space;> Risk
Treatment SHOULD be administered
Recommendation that treatment is useful/effective

52
Q

What is the ACC/AHA classification scheme class IIa?

A

Benefit&raquo_space; Risk
IT IS REASONABLE to administer treatment
Recommendation in favor of treatment being useful/effective

53
Q

What is the ACC/AHA classification scheme class IIb?

A

Benefit > Risk
Treatment MAY BE CONSIDERED
Recommendation’s usefulness/efficacy less well established

54
Q

What is the ACC/AHA classification scheme class III?

A

Risk > Benefit
Treatment should NOT be administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL
Recommendation that treatment is not useful/effective and may be harmful

55
Q

What are the initial recommendations for NSTEMI/UA and STEMI use of nitroglycerin (NTG)?

A

Take 1 SL NTG in response to chest pain/discomfort (if unimproved or worsened after 5 min call 911 (Class I)
Patients with ongoing ischemic discomfort should receive SL NTG q 5 min for a total of 3 doses (Class I)
After 3 doses assess for need for IV NTG (Class I)
IV indicated in first 48 hours for treatment of persistent ischemia, HF, or hypertension

56
Q

What are the STEMI indications for nitroglycerin?

A

Continued use of NTG beyond 1st 48 hours in absence of continued or recurrent angina or HF may be helpful although benefit likely small and not well established (Class IIb)

57
Q

What is the DOC for analgesia?

A

Morphine

58
Q

Morphine- MOA

A

Sedative properties tend to decrease anxiety
Causes venodilation
Vagal activity decreases HR and BP

59
Q

Morphine- NSTEMI/UA

A

Administer if there is uncontrolled ischemic chest discomfort despite NTG (Class IIa)

60
Q

Morphine- STEMI

A

Analgesic of choice for management of pain (Class I)

61
Q

What are the Fibrinolytics (Thrombolytics)?

A 
STREPTOKINASE
Anistreplase
ALTEPLASE
Retelplase
Tenecteplase
62
Q

Fibrinolytics (Thrombolytics)- STEMI uses (absence of contranindications)

A
  • Fibrinolytic therapy should be admin with symptom onset within the prior 12 hours and ST elevation greater than 1mm in at least 2 continguous precordial leads or at least 2 adjacent limb leads (Class I)
  • Or sx onset within prior 12 hours and presumably new left branch bundle block (Class I)
  • Sx onset within prior 12 hours and 12-lead ECG findings consistent with true posterior MI (Class IIa)
  • Sx onset within prior 12-24 hours who have continuing ischemic sx and ST elevation > 1mm in at least 2 continguous precordial leads or 2 adjacent limb leads (Class Iia- no good studies that show pas12 hours that there is benefit)
  • Fibrinolytic therapy should not be administered to patients whose initial symptoms began more than 24 hours earlier (Class III)
63
Q

ASA has a ____% reduction in mortality and MI rates?

A

50%

64
Q

Antiplatelets- NSTEMI/UA (Class I)

A
  • ASA (162-325mg) should be chewed by patients who have not taken ASA before presentation
  • Clopidogrel (plavex) should be admin to patients unable to take ASA
65
Q

Antiplatelets- Initial conservative strategy

A
  • Clopidogrel (plavex)should be added to ASA and an anticoagulant ASAP after admission and continued for at least 1 month ideally up to 1 year (doesn’t mean upon adminsion)
  • If recurrent sx of ischemia, HF, or serious arrhythmias subsequently appear then diagnostic angiography should be performed. Prior to performing angiography either an IV GPIIb/IIIa inh or clopidogrel should be added to ASA and an anticoagulant.
66
Q

Antiplatelets- Initial invasive strategy

A
  • Either clopidogrel (plavex) or an IV GP IIaIIIb inh should be added to ASA prior to diagnostic angiography
  • Abciximab (is the only IIaIIIB inhibitor apprioved is PCI is going down) is indicated here only if no appreciative delay in angiography and PCI is likely to be performed
  • Otherwise IV eptifibatide or tirofiban is preferred
67
Q

Do patients need to chew or swallow aspirin if having an MI?

A

CHEW IT

68
Q

Antiplatelets- NSTEMI UA

A

–(Class IIa)
Conservative
For patients with recurrent ischemic discomfort with clopidogrel, ASA, and anticoagulant therapy it is reasonable to add a GPIIaIIIb inh before diagnostic angiography
Invasive
Reasonable to admin antiplatelet with both clopidogrel and IV GPIIaIIIb inh. Abciximab only if no delay in angiography and PCI to be performed, otherwise eptifibatide or tirofiban are preferred
–(Class IIb)
For patients in whom an initial conservative strategy is selected it may be reasonable to add IV eptifibatide or tirofiban to anticoagulant and oral antiplatelet therapy
–(Class III)
Abciximab should not be admin to patients in whom PCI is not planed

69
Q

Antiplatelets- STEMI (Class I)

A

–ASA (162-325mg) should be chewed by patients who have not taken ASA before presentation
Clopidogrel should be admin to patients unable to take ASA
–Clopidogrel 75 mg should be added to ASA regardless of whether they undergo reperfusion with fibronolytic therapy or not. Treatment should continue for at least 14 days

70
Q

Antiplatelets- STEMI (Class IIa)

A
  • In patients < 75 years who receive fibrinolytic therapy or who do not receive reprofusion therapy it is reasonable to administer oral loading dose of clopidogrel 300mg
  • It is reasonable to start treatment with abciximab as early as possible before PCI
71
Q

Antiplatelets- STEMI (Class IIb)

A
  • Abciximab and half dose reteplase or tenecteplase may be considered for STEMI in selected patients: anterior MI, < 75 years; and not risk factors for bleeding
  • Treatment with tirofiban or eptifibatide may be considered before primary PCI
72
Q

Antiplatelets- STEMI (Class III)

A
  • Abciximab and half dose reteplacse or tenecteplase should not be given to patients aged > 75 years because of an increased risk of ICH
  • Full dose fibrinolytic therapy followed by immediate PCI may be harmful
73
Q

What do anticoagulants do?

A

Act to prevent thrombus formation

74
Q

Anticoagulants- NSTEMI/UA (Class I)

A

Anticoagulant therapy should be added ASAP

Conservative: Regimens with either enoxaparin or UFH have strongest data support followed by fondaparinux
In patients who have an increased risk of bleeding fondaparinux is preferable

Invasive: Enoxaparin and UFH have strongest support followed by bivalirudin and fondaparinux

75
Q

Anticoagulants- NSTEMI/UA (Class IIa)

A
  • If initial conservative strategy enoxaparin or fondaparinux is preferable to UFH unless CABG is planned within 24 hours
  • If initial invasive strategy reasonable to omit IV GPIIaIIIb inh prior to diagnostic angiography if bivalirudin is selected as anticoagulant and at least 300 mg clopidogrel admin at least 6h earlier than planned catheterization or PCI
76
Q

Anticoagulants- STEMI Class I

A
  • Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours and preferably for the duration of hospitalization, up to 8 days. Anticoagulant regimens with established efficacy include:
  • -UFH (up to 48 hrs)- heparin
  • -Enoxaparin (in the absence of renal dysfunction; continued for the duration of hospitalization, up to 8d)
  • -Fondaparinux (in the absence of renal dysfunction; continued for the duration of hospitalization, up to 8d)
77
Q

Anticoagulants- STEMI Class I for patients undergoing PCI after receiving an anticoagulant

A
  • For prior treatment with UFH, administer additional boluses as needed for the procedure. Bivalirudin may also be used.
  • For prior treatment with enoxaparin, if the last Sub Q dose was administered within the prior 8 hours, give no additional doses; if the last Sub Q dose was administered at least 8-12 hours earlier, give an IV dose of 0.3 mg/kg.
  • For prior treatment with fondaparinux, give additional IV treatment with an anticoagulant possessing anti-IIa activity.
78
Q

Anticoagulants- STEMI Class IIa

A

It is reasonable for patients with STEMI who do not undergo reperfusion therapy to be treated with anticoagulant therapy (non-UFH regimen) for the duration of theindex hospitalization, up to 8 days.

79
Q

Anticoagulants- STEMI class III

A
  • Because of the risk of catheter thrombosis, fondaparinux should not be used as the sole anticoagulant to support PCI. An additional anticoagulant with anti-IIa activity should be administered.
  • LMWH should not be used as an alternative to UFH as ancillary therapy in patients > 75 years of age who are receiving fibrinolytic therapy.
  • LMWH should not be used as an alternative to -UFH as ancillary therapy in patients < 75 years of age who are receiving fibrinolytic therapy but have significant renal dysfunction (serum creatinine > 2.5 mg/dL in men or 2.0mg/dL in women).
80
Q

Beta blockers- uses

A
  • -Limit myocardial damage and mortality when used for acute STEMI
  • -Reduce reinfarction and mortality when used chronically post-STEMI
  • -Begin with IV as indicated acutely, then switch to PO that same day. May start with oral in moderate to low risk patients
81
Q

Beta blockers- precautions

A
  • HR< 50bpm, Heart block, Hypotension (SBP< 100 mmHg), Mod-severe LV dysfunction, COPD, asthma, signs of peripheral hypoperfusion
  • If contraindications exist in acute MI setting, BB can and should be started late (If contraindications resolve) with PO therapy
82
Q

Beta blockers- NSTEMI/UA and STEMI class I

A

ORAL BETA-BLOCKERS therapy should be initiated within the first 24 h for patients who do not have signs of heart failure or evidence of a low-output state or other relative contraindications to beta blockade (heart block, active asthma, or reactive airway disease)

83
Q

Beta blockers- NSTEMI/UA and STEMI class IIa

A

It is reasonable to administer IV BETA BLOCKERS at the time of presentation for hypertensive patients who do NOT have signs of HF or evidence of a low-output state or other relative contraindications to beta blockade

84
Q

Beta blockers- NSTEMI/UA and STEMI class III

A

IV BETA BLOCKERS should NOT be administered to patients who have signs of HF or low-output state, risk factors for cardiogenic shock, or other relative indications to beta-blockade

85
Q

ACE inhibitors- MOA

A
  • Decrease progression to CHF, reinfarction, and mortality

- Limit post-infarction left ventricular dilatation and hypertrophy (remodeling) and preserve ventricular pump function

86
Q

ACE inhibitors- Uses

A
  • Patients with left ventricular ejection fractions < 40% may derive the most benefit
  • Therapy should begin ASAP
  • KEEP IN MIND: these patients will also be on a beta-blocker; therefore start the ACE inhibitor only when the patient is hemodynamically stable
87
Q

ACE inhibitors- NSTEMI/UA and STEMI class I

A

An ACE INHIBITOR should be administered ORALLY within the first 24 h to patients with anterior infarction, pulmonary congestion or LV ejection fraction (LVEF) < 40%, in the absence of hypotension (SBP < 100 mm Hg or < 30 mmHg below baseline)

  • An ANGIOTENSIN RECEPTOR BLOCKER should be administered to UA/NSTEMI patients who are intolerant of ACE inhibitors
  • An ANGIOTENSIN RECEPTOR BLOCKER should be administered to STEMI patients who are intolerant of ACE inhibitors and who have either clinical or radiological signs of heart failure or LVEF < 40%. VALSARTAN AND CANDESARTAN have established efficacy for this
88
Q

ACE inhibitors- NSTEMI/UA and STEMI class IIA

A

An ACE INHIBITOR administered ORALLY within the first 24 h can be useful in patients without anterior infarction, pulmonary congestion or LVEF < 40% in the absence of hypotension. The expected treatment benefit in such patients is less (5 lives saved per 1000 patients treated) than for patients with LV dysfunction

89
Q

ACE inhibitors- NSTEMI/UA and STEMI class III

A

An INTRAVENOUS ACE INHIBITOR should NOT be given to patients within the first 24 hrs because of the increased risk of hypotension. (A possible exception may be patients with refractory HTN)

90
Q

Calcium channel blockers- benefits and risks

A
  • No beneficial effect on death or nonfatal MI

- May increase mortality in some patient groups (LV dysfunction, Pulmonary Edema)

91
Q

Calcium channel blockers- NSTEMI/UA class I

A

In patients with continuing or frequently recurring ischemia and in whom BB are contraindicated Verapamil or Diltiazem should be given as initial therapy in absence of significant left ventricular dysfunction or other contraindications

92
Q

Calcium channel blockers- NSTEMI/UA class IIa

A

Long-acting Verapamil or Diltiazem are reasonable to use for recurrent ischemia in absence of contraindications after BB and nitrates have been fully used

93
Q

Calcium channel blockers- NSTEMI/UA class IIb

A

Use of ER Verapamil or diltiazem instead of a BB may be considered
IR dihydropyridine CCB in presence of adequate beta blockade may be considered in patients with ongoing ischemic sx or HTN

94
Q

Calcium channel blockers- NSTEMI/UA class III

A

IR dihydropyridine CCB should not be admin to patients with NSTEMI/UA in the absence of a beta blocker

95
Q

Calcium channel blockers-STEMI class IIa

A

It is reasonanle to give Verapamil or Diltiazem to patients in whom BB are ineffective or contraindicated for relief of ongoing ischemia or control of rapid ventricular response with afib after STEMI in absence of CHF, LV dysfunction, or AV block

96
Q

Calcium channel blockers-STEMI class III

A
  • Verapamil and diltiazem contraindicated in patients with STEMI and associated systolic LV dysfunction and CHF
  • Nifedipine IR form is contraindicated because of reflex sympathetic activation, tachycardia, and hypotension associated with its use
97
Q

Overall what should you give patients with NSTEMI/UA and STEMI?

A 
Give ASAP*
ASA- CHEW IT
NTG- sublinguial every 5 mins x 3 doses
Beta-Blocker
Ace Inhibitor
98
Q

What are the long term prevention CAD for NSTEMI/UA and STEMI?

A

ASA (use indefinitely)+ Clopidogrel length of Clopidogrel as follows:

NSTEMI/UA
No stent/bare metal stent: at least 1 month up to12 months
Drug eluting stent: at least 12 months)

STEMI
Bare metal and drug eluting as above
Thrombolytic at least for 14 days

99
Q

What is the long term prevention with NTG (Class I)

A

All patients should be given SL NTG

Long acting oral nitrates may be used to prevent ischemic symptoms

100
Q

What is the long term prevention with beta blockers class I?

A

(Class I) Are indicated for all patients recovering from ACS unless contraindicated (for those at low risk, see Class IIa recommendation below). Treatment should begin within a few days of the event, if not initiated acutely, and should be continued indefinitely.
Patients recovering from ACS with moderate or severe LV failure should receive BETA BLOCKER therapy with a gradual titration scheme.

101
Q

What is the long term prevention with beta blockers class IIa?

A

(Class IIa) It is reasonable to prescribe BETA BLOCKERS to low-risk patients (i.e., normal LV function, revascularized, no high-risk features) recovering from ACS in the absence of absolute contraindications.

102
Q

What is the long term prevention for ACE inhibitors class I?

A
  • Should be given and continued indefinitely in all patients recovering from ACS with HF, LV dysfunction (ejection fraction less than or equal to 40%), hypertension, diabetes mellitus, or chronic kidney disease, unless contraindicated.
  • An ARB should be prescribed at discharge to patients who are intolerant of an ACE inhibitor and who have either clinical or radiological signs of HF and LVEF < 40% It is beneficial to use an ARB in other patients who are ACE inhibitor intolerant and have hypertension.
  • Long-term ALDOSTERONE RECEPTOR BLOCKAGE should be prescribed for post-MI patients without significant renal dysfunction (estimated creatinine clearance should be > 30 mL/min) or hyperkalemia (potassium should be < 5 mEq/L) who are already receiving therapeutic doses of an ACE inhibitor, have an LVEF < 40%, and have either symptomatic HF or diabetes mellitus.
103
Q

What is the long term prevention for ACE inhibitors class IIa?

A

ACE INHIBITORS are reasonable for patients recovering from ACS in the absence of LV dysfunction, hypertension, or diabetes mellitus unless contraindicated.
In patients who do not tolerate ACE inhibitors, an ARB can be a useful alternative in long-term management provided there are either clinical or radiological signs of HF and LVEF less than 40%

104
Q

What is the long term prevention for ACE inhibitors class IIB?

A

The combination of an ACE INHIBITOR and an ARB may be considered in the long-term management of patients recovering from ACS with persistent symptomatic HF and LVEF < 40% despite conventional therapy including an ACE inhibitor or ARB alone.

105
Q

What is the long term prevention for HMG- CoA reductase inhibitors?

A

-Decrease cardiovascular mortality and all-cause mortality in patients with a variety of cholesterol concentrations
-Hypercholesterolemic patients benefit most, but patients with normal cholesterol levels also benefit
Good for both primary (prevents first event) and secondary (prevents recurrence of an event) prevention of myocardial infarction

106
Q

What is the long term prevention involving statins class I, IIA, and IIB?

A

(Class I) Statins, in the absence of contraindications, regardless of baseline LDL-C and diet modification, should be given to post-ACS patients
For patients with LDL-C > 100 mg/dL, cholesterol-lowering therapy should be initiated or intensified to achieve an LDL-C of < 100 mg/dL.

(Class IIa)
Further reduction of LDL-C to < 70 mg/dL is reasonable.

(Class IIb)
Encouraging consumption of omega-3 fatty acids in the form of fish or in capsule form (1 g per d) for risk reduction may be reasonable. For treatment of elevated triglycerides, higher doses (2 to 4 g per d) may be used for risk reduction.

107
Q

What is long term prevention class I?

A
  • Calcium channel blockers are recommended for ischemic symptoms when beta blockers are not successful, contraindicated, or cause unacceptable side effects.
  • Verapamil and diltiazem are preferred in the absence of severe left ventricular dysfunction or other contraindication.
108
Q

What is long term prevention class III?

A

(Class III) Short-acting dihydropyridine calcium channel antagonists should be avoided.

109
Q

Warfarin class I

A

Managing warfarin to an INR (internationalized ratio for how fast the blood clots, normally want to be between 2-3 seconds) equal to 2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter is recommended, and in post-MI patients when clinically indicated (e.g., atrial fibrillation, left ventricular thrombus)

110
Q

What is the target INR for patients on warfarin, clopidogrel, and aspirin?

A

In patients requiring WARFARIN, CLOPIDOGREL AND ASPIRIN therapy, an INR of 2.0 to 2.5 is recommended with low dose aspirin (75 mg to 81 mg) and a 75 mg dose of clopidogrel.

111
Q

What is the use of WARFARIN in conjunction with ASA and/or CLOPIDOGREL associated with an increase of?

A

Use of warfarin in conjunction with ASA and/or clopidogrel is associated with an increased risk of bleeding and should be monitored closely

Pharmacology II (23 decks)

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